دورية أكاديمية
No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia.
| العنوان: | No evidence so far of a major role of AKT1 and GSK3B in the pathogenesis of antipsychotic-induced tardive dyskinesia. |
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| المؤلفون: | Levchenko A; Institute of Translational Biomedicine, Saint Petersburg State University, Saint Petersburg, Russia., Vyalova N; Tomsk National Research Medical Center of the Russian Academy of Sciences, Mental Health Research Institute, Tomsk, Russia., Pozhidaev IV; Tomsk National Research Medical Center of the Russian Academy of Sciences, Mental Health Research Institute, Tomsk, Russia., Boiko AS; Tomsk National Research Medical Center of the Russian Academy of Sciences, Mental Health Research Institute, Tomsk, Russia., Osmanova DZ; Tomsk National Research Medical Center of the Russian Academy of Sciences, Mental Health Research Institute, Tomsk, Russia., Fedorenko OY; Tomsk National Research Medical Center of the Russian Academy of Sciences, Mental Health Research Institute, Tomsk, Russia.; Division for Control and Diagnostics, School of Non-Destructive Testing & Security, National Research Tomsk Polytechnic University, Tomsk, Russia., Semke AV; Tomsk National Research Medical Center of the Russian Academy of Sciences, Mental Health Research Institute, Tomsk, Russia., Bokhan NA; Tomsk National Research Medical Center of the Russian Academy of Sciences, Mental Health Research Institute, Tomsk, Russia.; Department of Psychotherapy and Psychological Counseling, National Research Tomsk State University, Tomsk, Russia., Wilffert B; Unit of PharmacoTherapy, Epidemiology and Economics, Groningen Research Institute of Pharmacy, University of Groningen, Groningen, The Netherlands.; Department of Clinical Pharmacy and Pharmacology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands., Loonen AJM; Unit of PharmacoTherapy, Epidemiology and Economics, Groningen Research Institute of Pharmacy, University of Groningen, Groningen, The Netherlands.; GGZ Westelijk Noord-Brabant, Bergen op Zoom, The Netherlands., Ivanova SA; Tomsk National Research Medical Center of the Russian Academy of Sciences, Mental Health Research Institute, Tomsk, Russia.; Division for Control and Diagnostics, School of Non-Destructive Testing & Security, National Research Tomsk Polytechnic University, Tomsk, Russia. |
| المصدر: | Human psychopharmacology [Hum Psychopharmacol] 2019 Jan; Vol. 34 (1), pp. e2685. Date of Electronic Publication: 2019 Jan 08. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Wiley & Sons Country of Publication: England NLM ID: 8702539 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1099-1077 (Electronic) Linking ISSN: 08856222 NLM ISO Abbreviation: Hum Psychopharmacol Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Chichester, Sussex, England : Wiley & Sons, c1986- |
| مواضيع طبية MeSH: | Antipsychotic Agents/*adverse effects , Glycogen Synthase Kinase 3 beta/*physiology , Proto-Oncogene Proteins c-akt/*physiology , Tardive Dyskinesia/*chemically induced, Adult ; Female ; Glycogen Synthase Kinase 3 beta/genetics ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins c-akt/genetics ; Receptors, Dopamine D2/physiology |
| مستخلص: | Objective: AKT1 and GSK3B take part in one of the intracellular cascades activated by the D2 dopamine receptor (DRD2). This receptor is antagonized by antipsychotics and plays a role in the pathogenesis of antipsychotic-induced tardive dyskinesia (TD). The present study investigated association of several polymorphisms in the two candidate genes, AKT1 and GSK3B, with TD in antipsychotic-treated patients with schizophrenia. Methods: DNA samples from 449 patients from several Siberian regions (Russia) were genotyped, and the results were analyzed using chi-squared tests and analyses of variance. Results: Antipsychotic-induced TD was not associated with either of the tested functional polymorphisms (rs334558, rs1130214, and rs3730358). Conclusions: Despite regulation of AKT1 and GSK3B by DRD2, we found no evidence that these two kinases play a major role in the pathogenesis of antipsychotic-induced TD. These results agree with previously published data and necessitate further exploration of other pathogenic mechanisms, such as neurotoxicity due to excessive dopamine metabolism. (© 2019 John Wiley & Sons, Ltd.) |
| معلومات مُعتمدة: | 30 International Siberian Branch, Russian Academy of Sciences |
| فهرسة مساهمة: | Keywords: AKT1; GSK3B; antipsychotics; pharmacogenetics; schizophrenia; tardive dyskinesia |
| المشرفين على المادة: | 0 (Antipsychotic Agents) 0 (Receptors, Dopamine D2) EC 2.7.11.1 (AKT1 protein, human) EC 2.7.11.1 (GSK3B protein, human) EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) |
| تواريخ الأحداث: | Date Created: 20190110 Date Completed: 20200312 Latest Revision: 20200312 |
| رمز التحديث: | 20240628 |
| DOI: | 10.1002/hup.2685 |
| PMID: | 30623492 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1099-1077 |
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| DOI: | 10.1002/hup.2685 |